Amoebic dysentery - DigitalCommons@UNMC

University of Nebraska Medical Center
DigitalCommons@UNMC
MD Theses
College of Medicine
5-1-1934
Amoebic dysentery
H. C. Dix
University of Nebraska Medical Center
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Dix, H. C., "Amoebic dysentery" (1934). MD Theses. Paper 320.
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A MOE B l e D Y SEN T E R Y
By
H.
c.
Dix
University of Nebraska
College of Medicine
Omaha, N~braska
April 1934
Preface
This paper is presented to the University of
Nebraska College of MediCine to fulfill the senior
requirements.
The subject of amoebic dysentery wa,s chosen due
to the interest aroused from the previous epidemic,
which started in Chicago la,st summer (1933).
This disea,se has previously been considered as
a tropical disease, B.nd was rarely seen and recognized
in the temperate zone.
Except in indl vidu8,ls who had
been in the tropics previously.
In reviewing the literature, I find that amoebio
dysentery may be seen in any part of the world, and
from surveys made, the incidence is five in every hundred which harbor the Entamoeba histolytlca, it being
the only pathogeniC amoeba of the human gastro-intestinal tract.
This disease is one of great importance and should
be more thoroughly understood by the medical profession
than it has in the past.
One reason for this is that
it is important to treat carriers, and the profession
should be able to recognize these individuals, which
is the all-important factor in control of the disea.se,
and I hope that this paper will be of some aid to its
readers in making a. diagnosis a,nd being a,ble to
this disea.se.
ha~ndle
H. O. Dix.
-1-
Amoffbic Dysentery
History
The Amoeba histolytlca was first discovered in
1859 by Lambl (1) in the stools of a child suffering
from enteri tis, but he did not think of" pa,thogenic
importance.
They were again noted some years later,
both by Cunningham 8"nd Lewis, in the stools of cholers.
patients, and even in the stools of apparently hea.lthy
i ndi vi duals.
The name Amoeba Ooli was first conferred by Losch,
who in 1875 found the organisms in the stools of a chronic dysenteric patient, who at necropsy, waS found to
have extensive ulceration of the colon.
He claimed
for them, in part only, an etiological relationship
with dysentery.
He described them minutely as to shape,
size, and character of motility.
Losch attempted to produce the disease in dogs.
Be injected the fecs.l material conts"ining the amoebae
into the rectum of four dogs.
In one of them eight
days later he found amoebae in the stools, and in another, which
W~lS
ki lled on the eighth day, he found
rectal swelling, injection and slight ulceration.
Kruse and Pasquale 8.1so injected fecal material
in the rectum of dogs and retained it by suturing the
anus and they produced
di tion found in man.
B"
condi tion similar to the con-
Tbey also used necrotic materia.l
-2-
from a secondary liver abscess and produced
8.
condi-
tion similar to that found in man which waS the first
proof that secondary liver a.bscesses contained the
amoeba,.
Marchaux succeeded in producing the disease in
cats, those having lived over fifteen days developed
sec0!ldary Ii ver abscesses, "usually single".
Robert Koch was the first man to really give
definite knowledge of its parasitic properties.
While
investigating cholera in Egypt in 1883, he found the
amoeba in the deeper portions of the ulcers in the intestines of several cases of dysentery, 8.nd because of
their deep position, he looked upon them 8,S exciting a
causal relationship.
It was his influence that caused
,Kartulis to study them.
Kartulis in 1885 started his work on the disease.
He found amoebae in the stools of five hundred cases
of dysentery in Egypt, and also found them in the necrotic contents and wall of liver abscesses complicating
the disease.
He o-oserved, too, ths,t their number was
seemingly related to the severity of the attack.
He
also failed to find amoebae in other cases of dysentery
other ths,n amoebic dysentery.
They noted that amoebae
were found in patients of other dises,ses such as cholera.
and also
a,pp~lrently
normal individuals.
-3-
Osler, in 1890, WeB the first man in the United
States to report the finding of amoebae in the stools
and hepatic abscesses of a case of amoebic dysentery_
His patient came from the Panama Canal Zone.
The finding of amoebae in stools of normal individuals and of those ill with other conditions than
dysentery, and the fa,ct theot rectal injections in 8,nimals sometimes failed to produce dysentery in them,
led to the question whether the amoeba waS really pa,thogenic or whether more than one variety existed, one
type being pathogenic and the other non-pathogenic ..
Several observers hed reported the finding of
amoebae which were larger than tha.t described by Losch
as Amoeba Coli, a,nd presenting a. different encysted
form.
Quineke B.nd Roos were among the first, who en-
deavored to show that variations doubtless exist. With
one type they succeeded in inducing, in cats, both
dysentery and Ii ver abscesses, while the amoeba,e from
another source failed' absolutely.
The\T also describe
an intermediate type which caused mild intestina.l symptoms when injected by rectum into cats.
This led them
to name these Amoeba. Ooli, retaining the name by Losch
to that type inducing most severe results, and Amoeba,
i
Coli Mitis, the mild variety and Amoeba Coli Vulgaris,
the non-pathogenic
type.~
These later they obtained
-4-
from the stools of normal individuals after the administration of carlsbad salts, finding amoebae in 9 out
of 24.
Schulberg found them in 10 out of 20 in liquid
stools of' normal individuals, but fai led to find them
in normal individuals.
Calandruccio swallowed amoebae and though he continued to find them in his stools for some days, no
marked condition resulted.
Then Oounci lman a)ld Lafleur (3) started to change
the previous classifica,tion and put them under pathogenic and non-pathogenic types.
The pathogenic form
was termed Ameba, dysenteriae and the non-P8cthogenic,
Amoeba Coli.
This classification lasted up until the
time of Schaudinn in 1903.
After his experiments he
termed the non-pathogenic type of amoeba "Entameba
Coli ft and the pathogenic "Entameba histolytic8,11 and
this term has been unchanged up to the present time.
Soon after Schaudinn had printed his paper and given
the new classification, Viereck, in 1907, described a
third form which
WaS
called EntE>.meba tetragena, but not
unti 1 1913 was the identi ty of Enta.meba tetragena and
Entameba histolytica brought out.
So by this it waS
concluded that there was only one pathogenic form and
this was Entameba, histolytica,.
The family history is
given by both Schaudinn and iJiereck.
Due to the work of Walker (2) in 1911, and Mathis
in 1913, and many others, we have been lea.d to turn
-5-
from the trophozoite form to the study of cysts which
waS described at this time •
. Rogers, in 1912, introduced the use of emetine.
Emetine had been used many years before.
In 1891,
Tull, Walsh a.nd Warden had found the total alkaloid
of
epec~lcuanha.
The emetine of that period cured
cases of dysen'tery which were uneffected by epecacuanha depri ved of the a,lkaloid emetine, but this 'tVa.S
forgotten for some time, until when amoebic dysentery
was differentiated from bacillary dysentery.
waS rediscovered.
Then it
This waS impressed when Vedder ob-
served that the growth of free-living amoeba was inhibi ted by high d,i lutions of emetine and cephoeline,
and when Rogers descri bed the immobili ty and de£tth of
Entameba hlstolytlca obtained from dysenteric stools,
by contact with a solution of emetine hydrochloride
one part to one hundred thousand.
In the years from 1912 to 1916 there Wa,s considerable progress made in the identification and classification of the different types of amoeba,e.
In 1919 to 1920 Dr. Craig (5) worked out the
complement fixation reaction which Was of some aid
in diagnosis.
In 1921 an a,rticle was published by Kofoid and
Swezy (6) on the effects of amoebiosis on a.rthri tiS,
therefore considering the disease as a systemic disease.
-6-
There has also been some recent work and many
publications made since the recent epidemic in Chicago, which has made the United States amoebic minded.
Many new staining processes have been developed and
culture medium has been changed, but in trying to culture the parasites, it has been very difficult to get
growth.
-7-
Epidemiology
Amoebic dysentery is cha,racteristically an endemic disease, which is primarily of the tropics and
subtropics, but a,t the present time, it is tInown to
be where every man may live.
The cysts are undoubted-
ly the propoga,ti ve stage of the entamebae.
It is al-
ways necessary for a, pa,rasi te to be able to lea,ve a
host and then re-infect a new host without being killed.
The cyst being qui te resistant, carries out the externs,l
part of the life cycle of this perasite.
No multiplici-
ty of the cysts or
tropho~oi tes
ts"kes place out side of
the host (7).
tropho~oi tes
degenerate very ra,pidly
The
outside the host, and if the trophozoite is taken into
the host by mouth, it will not set up any infection due
to the fact tha,t it can not resist the digesti ve action
of the secretions of the stomach.
The cysts being quite
resistant a,re not destroyed when taken in wi th food,
but set up an infection very rea,dily. In some cases symptoms develop, while in others no symptoms appear, but
virulent cysts are passed in the stools.
In this way
the individual becomes a, very serious menace to society.
In handling dejecta of son amoebic dysentery pa,tient
it should always be destroyed in a manner which will kill
all trophozoi tes and cysts.
m.a,y show only the
v:'f/,41A:ri,~e
The eXB,mination of the stool
forms, but you never know when
cysts will appear in the stool in large quantities.
-8-
The causative fa.ctor producing excystation of
the vefl'titltve form is unknown.
Certainly warmth and
moisture axe necessary, nutrient matter and enzymes,
singly or in conjunction with each other, may be essential factors.
The life cycle is of great value in
showing the infective stages.
Life cycle of Entameba histolytica (8).
It 1s
comparatively Simple, consisting of two distinct stages.
The trophozoi tes being the vegAr,,'fl\le stage.
They
multiply and are motile, being f'ound in the intestinal
tract, producing lesions
a~nd
symptoms of the disease.
The moti Ie forms are passed in la,rge numbers in
the feces, but are destroyed in a short time after
leaving the body, and when ingested, are destroyed by
gastriC juice and secretions of the jejunum.
In the
course of an established infection, condi tions unfa.vorable for growth eventually develop.
The exa,ct na-
ture of these unfavora.ble cond! tions is sti 11 obscure.
The trophozoi tes cea,se to ingest food, "which is red
blood cells to a great extent", round up, become motionless and filled with glycogen.
The size diminishes
and newly formed cysts containing one nucleus 8.re found.
This signifies the immature cysts..
Then the nucleus
divides and two nuclei are present, and the two nuclei
divide once more giving four nuclei.
cyst ~
This is a mature
Many of the cysts seen in the feces 8,re immature.
-9-
They vary in size from about seven microns to fifteen
microns.
As previously stated, the propaga.tion from one
host to another is entirely dependent upon the· cysts.
When the acute symptoms subSide, some of the trophozoites in the colon usuldly und.ergo encystment.
These
cysts pass out in the feces and these cysts B,re qui te
reSistant, but when ingested by mouth, excystation
occurs in the small intestine and colon, a four nucleated amoeba emerges from the cyst or four small amoebao.
"This is not definitely known."
These amoeba are a.r-
rested at points of stasi s in the la.rge bowel.
They
penetrate tbe mucosa and form the typical lesion of
amoebic dysentery.
Dr. Hegner (9) while in Pa,nsma did many very interesting experiments on the life cycle of the Entameba histolytica.
He and his associates worked with
the trophozoites of Entamoeba histolytica from human
cases of acute intestinal amoebiosis.
He gives a new classification of the different
types of Entameba histolytlca based upon morphology
and locomotion.
Type one is the tissue invading amoeba,
two is the precystic amoeba, and third the cysts.
He describes the tissue dwelling amoeba as occur
in the mucosa, submucosa and even in the muscular layers.
The term Lumen Amoebae is proposed.. for a second
type which lives in the lumen of the intestine.
-10-
It is
usually assumed that amoebae enter the tissue where
they multiply rapidly.
Some of the offsprings pass
out into the lumen where they become the precystic
type and a.re evacuated in the feces.
The tissue dwelling amoeba.e are loca.ted at the
base and the sides of the ulcers and not in the exudate
and none were seen in the material on the way out of
the ulcers.
It seems hardly possible for the enormous
number of amoebae in the lumen to originate from the
comparatively few tissue dwelling amoeba,e •
..-
In carriers where there are few is-/any tissue
dwelling amoeba,e, so Dr. Hegner thinks, there is reproduction of the trophozoites in the lumen and not
all amoibae are from tissue dwelling amoeba,e.
Precystic a.moeba. e are lumen a,moebee that for some
unknown reason, I1probably some unfavorable condition",
has been stimulated to encyst.
A few precystic amoebae
may origina"te in the tissues, but
mo~t
of them 8.re from
the lumen amoebae.
The cysts are of particular interest to those engaged in publiC health work because they are recognized
as the effective stage that ms,y set up a.n infection
when swallowed by a susceptible host.
A number of pro-
blems involving cyst were studied by Hegner, which included their development outside the body, and places
where excystation occurs.
The time required for ex-
cystation and the excysta.tion of immature cysts.
-11-
Development of cysts Qutside the body.
Material
from a stool containing la.rge numbers of cysts of Entameba histolytica was fexed
~nd
injected into the in-
testine of monkeys at defini te intervals, a.,nd this
showed evidence tha.t ei ther a differential destruction
of cysts occured or else development from uninucleated
cysts.
Time required for excysta,ti0:tl.
Entamoeba histo-
lytica cysts were injected into monkeys orally.
One
monkey was killed in two hours and twenty minutes, a
second in two hours end a half, and a third in three
hours.
Exc~Tstation
had begun in the first two, but
was well under way in the third monkey.
This shows
that excystation occurs in about three hours a.fter the
cysts are taken into the gastro-intestinal tract.
The plEtCe of excystation is largely in the sms.ll
intestine and also in the proxima,l portion of the colon.
Hegner could not get excysta,tion to occur by rectal injection of monkeys, as was reported in kittens by Bellard and Thei ler in 1924 and Hoore in 1925.
The. process of excystation.
The first sign of
excystation is the movement of the organism within the
cyst, then a, break occurs in the cyst wall and part of
the cyst flows out.
The cytoplasm flows in a.ga.in and
out and in a number of times before the organism actually escapes from the cyst.
-12-
The exc!station of immatu!£, cysts.
Amoeba car-
riers frequently pass large numbers of cysts containing only one or two nuclei.
It seems certain tha.t
cysts in any stage of development a.re ca.pable of excystation and hence infective to susceptible hosts.
It is not known if these cysts reach the stage of maturity or not before excystation, but it has been proven the.t a host can become infected from the ingestion
of immature cysts.
Much expe'rimental work has been done on this subject, and there is evidence to show that excystation
may even occur in the descending colon.
But many men
argue against this so there is no definite proof as to
the exact location of excystation.
Immunit!.
rne infection of the Entamoeba histo-
lytica affords no resistance to a. re-infection.
patients a,re prone to relapses. (10)
The
Although there
seems to be some racial resistance to the complications
of the infection, it
hSJ3
'oeen noted that in the nat,.Ve
people of the tropics, there is much less liver abscess
in per centage of cases than there is in the people of
the temperate zone.
The reason for this is unknown
un-
less the natives have aCQuired some natural immunity
over the centuries ths. t this disease has been prevelent
in the tropics.
The disease is much more prevelent in
the temperate zones in recent years, probe.bly due to
-13-
the rapid transportation and the much more intermlngl-.
ing of races in the last few centuries.
Prophylaxis.
There is no method of specific pro-
tection against amoebic infection.
The personal meas-
ures depending upon indl vidual cleanliness B.nd hygienic
precautions are important.
The prophylactic mea,sures have become
blem of the publiC health departments.
B.
great pro-
They' have the
problem of proper disposal of sewage which is a great
factor in the protection of the people, also in the
proper installment of plumbing as was brought out in
the Hotel in Chicago this summer. (11).
Another very important measure in prophylaxis is
the routine stool
examin~ttion
public boarding houses.
Of all food ha,ndlers in
The fala,cy in this is that
many cases of amoebiosis which present no symptoms will
not show cysts in all stools.
Therefore, they should
be examined at least once every three weeks for five
consecutive times.
In cases of dysentery with acute symptoms, the
stools should be burned or sterilized with some es,ustic
before disposed of.
All cS,ses of this type should have
periodic stool examinations for a year before a cure
is pronounced.
-14-
Morbid Anatomy
The gross appearance which the colon presents in
all the cases of amoebio dysentery varies oonsiderably
in oharaoter in different oases and even in the same
intestine.
There a.,re oertain features whioh
wi th in all O!lSeS"
8~re
met
The most striking chars,cteristic
in all, and the area whioh a.ttracts the etten tion to
this as a speoial anatomical form of dysentery,
the great thiokness of the intestine.
WaS
This is present
in every case, being much more ms.rked in some cases
than in others.
Sometimes the thickening involves a,ll
the ooats, while in other cases it is confined to the
submuoosa, and is alwa.ys most marked in the submuoosa.
There is not only a general thickening due to edematous
oonditions, but there are found Sharply circumscribed
projecting nodular thiokenings filled with gelatinous
looking pus.
These oavities communicate with the sur-
face of the mucous membrane by a small opening.
There
are also sinus traots, sometimes representing an extension of the cavi ty, anet sometimes oommunioating with
neighboring oavities of the same type.
The elevated
nodules varied considers,ble in size s.nd the openings
were frequently no It'rger than the hes,d of a small pin,
or so ltlrge that the cavi ty
WaS
freely exposed.
Even
then the surrounding mucous membrane was deeply undermined, and there were often found sinuses in the sub-
-15-
mucosa leadinf;: off from the ulcers.
These ulcers were filled with the Same glairy,
gelatinous-looking material as in the cavities. This
can be lifted out and leave the ulcer clean, but sometimes portions of it mes sti 11 cling to the wall.
The microscopic examine,tion nea,rly always contains
numbers of amoebae, red corpuscles, very round swollen
cells and pus cells.
single nucleus.
These large round cells have a
They are sometimes ,simply granular,
others are filled with fat drops.
They are probably
enlarged connective tissue cells which have become free
by softening of the tissue around the cells.
The whole
material is quite tenacious.
The undermined ulcers in connection with formation
of cavi ties end sinuse tra,cts in the submucosa, Can be
regarded
E1S
the form most frequently seen.
They are
found in th.e same intestine in connection wi th other
forms of ulcers, ano in some ca.ses are much more prominent than others.
They are most commonly seen in
the transverse ano descending colon.
In every case observed by
Councilm~
the submucous coat was the most affected.
infiltrated and
edema~tous,
and Lafleur,
This Was
not only in the neighbor-
hood of the ulcers, but in places which were free from
ulcers.
The ulcers increased in extent by the gradual
infiltration and
sof~ening
of this tissue with subse-
-16-
quent necros(s of the tisue immediately next to it.
The roof which covers the more or less closed ulcer
is broken tl1rough.
The infiltration and softening
continues at the Sides, and an ulcer with deeply undermined edges is formed.
The base of these ulcers 8re
cleaned and formed by the muscular coat.
Although
the ulcer advances in the submucosa by gra,dual softening and diSintegration of the tissue, the muscular
coat offers a barier to this cellular distruction. The
upper la,yers become necrotic, the cellular infiltration
extends into the muscle along the connective tissue between the bundles of muscular fibers, but it holds together.
The infi 1 tra,tion gradually extends through
into the intermuscula,r connect! ve tissue septa and the
subserous coat, and the same process is repeated here
as does in the submucosa.
The Circular muscular layer
is destroyed and the vessels supplying this
aree~
are
\
necrosed.
Kofoid and Swezy published an a,rticle in 1925
showing sections of the colon adja,cent to Bcn ulcer,
outSide the muscularis in the capilltuies and small
blood vessels of the serosa"
abundant evidence tha.t the
a,moebae have entered the blood strea,m and are thus in
a position to find their way in the hepatic portal system to the Ii vel' •
They a,lso showed the trophozoi tes
in the area around the ulcers.
-17-
Dr. Boeck ha,d, the op-
portuni ty of observing severs,l progressi ve stages in
the early invasion, as well as the gradua.l and ultimate destruction of the lymph follicles liS afforded
by lesions occuring in Peyer's patches of the terminal
ileum of fi ve kittens.
These amoebae showed 8,n appar-
ent selective action in attE:tcking the follicles, a,s
was evident from an initial necrosis of the epithelium
covering the tip of the follicle.
The adjacent epithe-
lium of the intestinal mucous gland was not 8,ffected.
Following the destruction of the epithelium over the
follicle, the amoebae moved down into the follicle,
a,nd the sinus tract W8_S formed.
The lymphoid cells of the follicle and the interstitial cells of the reticulum underwent necrosis. The
nuclei became pyknotic and the cytoplasm underwent dissolution.
There was practically no evidence of any
cullulsor reEtction to the infection in the
e~trly
stages
of the invasion, 'but later stages showed an infiltra.tion
of the submucosa at the outer limits of each follicle
with plasma cells chiefly, scattered polymorphonuclear,
,
large mononuclear, and a proliferation of connective
tissue elements attemptmng to wall off the lesion. In
the center of the gland there was progressive destruction of the lymph cells by the amoeba,e, resul ti ng in
much cellular detritus.
-18-
The amoebae, a,s they multiplied and formed a, local
8,bscess,
appe~tred
as large cells.
The abscess thus pro-
duced continued to grow until the whole follicle was
destroyed.
Later the mucosa overlying the abscess in
the submucosa may, in some cS,ses, slough off and produce a large deep ulcer.
The follicles in the colon also showed early inva,sion by amoebae.
This may go on simultaneous wi th
the invasion with the erosion destruction of the mucOSa a,djacent to the follicle or elsewhere, depending
upon location of the amoebic invasion.
This invasion
of lymphoid. follicles was also noted in the colon and
ileum in human cases reported by Councilman a.nd Lafleur.
luenen was the first to report a case which died of
perforation of the ileum by amoebic invasion of Peyer's
pa,tches.
Kofoid, Bayers and Swezy, in 1922, reported several
cases of Hodgkin's disease confirmed by pathological
examination of excised glands.
These gla,nds conta,ined
cells which supposedly were Entamoeba histolytica.. They
also report finding and demonstrating amoebae in several
cases of arthritis deformans.
-19-
Symptoms.to logy
The onset of symptoms of amoebic dysentery may
be very sudden or very insidious.
In the symptoms usually following an acute attack
the patient usually come under observation in the following condi tion:
Slightly emacis,ted and blanching of
the mucous membranes,muscular weakness, decubitus indifferent, expression dull, sensorium cles.r, skin often
dry and inelastic, distinctly
sa.llo~
tongue pale and
flab'by, moist and, more or less, fevered.
The abdomen
is of normal appearance or retrs.cted, tempera.ture not
usually s.bove 1000 F., often being normal, pulse ranging from 70 to 90, respirations from 18 to 30, appetite
impaired, and sleep disturbed by more or less freauent
evacuations of the bowels. (13)
A departure from or accentuation of certain features
in this clinical picture is observed in grave or in chronic dysentery.
In the gra,ve si tuation, the IS tient is
more or less prostrate, the f ace is drawn, slightly cyanosed or flushed and the expression anxious, mind usually quite clear, almost complete anorexia, intense
thirst and sleeplesness, abdomen greatly retra,cted and
there may be free sweating.
ly norms"l or subnormal.
The temperature is frequent-
The pulse is small and rs,pid
snd respirations proportionately accentuated.
In the chronic dysentery, the progressive a,nemia
and loss of flush are special features, which dominate
-20-
the intestinal symptoms.
The skin is dry, harsh and
of a dull grayish-yellow color.
The anemia which is present in a.ll cases of dysentery, deserves special mention.
The defeciency exists
both in the corpusclar elements and in the hemoglobin
in about the seme proportions.
It is, no doubt, to be
attributed partially to direct loss of blood in small
quantities from the intestinal tract and the rest is
attributed to mal-nutrition, but this does not ex.plain
the anemia occurring in chronic cases where the appetite
and nutrition is comparatively good and haS not lost
any appreciable blood by rectum.
tha~t
So it is considered
it is pa,rtly due to the ingestion of corpuscles
by the amoeba,e.
Diarrhea in some cases is the principal and only
feature of disease.
It is subject to great variation
in character and frequency.
The occurrence of inter-
mission and exacerbation has been noted as very characteristic.
This is the special characteristic of the
The exacerbation often begins suddenly a.nd subsides in the same manner, lasting from one to two days,
up to a week to ten days, and are progressively more
severe and longer duration in fatal ca.ses.
-
,
The intermissions have a wide range of duration,
.
from one day to three weekS, and during this time the
-21-
feces are soft or even formed, but mucous is usually
adherent to them.
It has t>een observed that the inter-
missions and exacerbations were most marked in C!tses
complicated by liver abscess.
The involvement of the liver does not coincide
wi th a.ny exa.cerbation of intestinal symptoms.
On the
contrary, as may be seen by reviewing case reports,
there is at this time ei ther a continuous diarrhea" of
moderate severity or slight loseness of the bowels alternating with constipation, and exacerbations occur
many days after there was evidence of hepatic or pulmonary involvement.
In Gangrenous dysentery, they may a.t first number
thirty to forty bowel movements in the first twentyfour hours, but subsequently the decline to from twelve
to eight or even to three or four at the end of a, fa.tal
case.
This may be due to a gradual loss of expulsive
power in the bowel.
The amount voided et each movement of the bowels
is at first sms,ll and often consists entirely of clear
masses of mucous mixed with more or less bright bloody
and occasionally small fecal masses.
As ulceration
a,dvances the stools become more copious, watery, and
less homogeneous, 'blood is less frequently observed
and small shreddy masses of a grayish or light yellow
color appear, mixed with blood-stained mucous.
-22-
When extensive sloughing takes place the character of the stools is even varied.
They are of a. gre.y-
ish, greenish (resembling spinach or green scum seen
in stagnant water), reddish brown or variegated color.
Sometimes quite liquid, at other times pultaceous, and
have a very penetrating offensive odor, mixed with finely divided shreddy detritus, mucus and streaks of dark
blood.
There are seen larger, tough stringy ma,sses of
necrotic tissue of a grayish or yellowish brown color.
No characteristica,lly purulent stools are passed, but
the same what slimy, gray, liquid movements conte.in
more pus cells than any other.
In dysentery of moderate severety of abrupt onset,
the stools are for a week to ten days similar to that
of gangrenous dysentery.
If the onset has been gradual
liquid brownish-yellow stools containing mucus, streaks
of blood, and many of the gelEJtinous grayish masses are
found.
Of this type there a,re usually four to ten stools
in twenty-four hours, and a flux of this degree, but
more irregular and without blood may continue for weeks.
In stools of chronic dysentery, they have a. more
homogeneous 8.ppearance.
They are watery or of the cori-
sistency and appearance of a thin gruel and of an earthy
or a dull yellow color, and conta.in few or many particles
.-
of clear mucus.
During an acute exacerbation, blood and
greenish, pultaceous materiel may be seen.
In intermis-
sions the stools may be formed or soft, but a.lso
-23-
8.
pres-
ence of mucus.
The rea.ction of dysentery stools is usua.lly alkElline which is thought to be due to protein putrefa.,otion.
Abdominal symptoms:
constant symptom.
Abaominal pain is the most
It occurs most frequently in the
ea,rly stages of gangrenous dysentery and dysentery of
moderate severity with an abrupt onset with acute exacerbations, with the subsidence of the acute diarrhea,
the pain decreases in severity, but, as it often disappears enti:rely as gangrene progresses, this does not
have a prognostic va,lue except in conjunction wi th other
fs,vora,ble symptoms.
In chronic cases,severe colic is not complained
of, except during exacerbations, but this is often a
dull aching or burning pa,in and a sensation of weight
about the epigastrium.
The pain is described by the
patient as cramp-like, teaJ3ing or sometimes burning.
It usua.lly precedes or accompanies the movement of the
bowels, when it is severe it is general, but subsequently is localized, usually to the lower abdomen.
Sensation to pressure is present in mEmy cases.
It is elicited most frequently by pressure along some
pa,rt of the course of the colon.
Tenesmus.
Great importance seems to have been
attached to this symptom, which is conSidered patho-
-24-
manic to some doctors, and, no doubt, is so of catarrhal dysentery and of most cases of diphtheritic
dysentery.
Dr. Councilman and Lafleur's observations
in the amoebic form of dysentery, however, coincides
with those of Dutraulu who noted the infrequency of
tenesmus in an extended series of cases of tropical
dysentery.
In Drs. Councilman and Lafleur's series of
cases tenesmus was noted in four cases and it is to be
observed that three of these were gangrenous forms of
dysentery, which is Boga,in in accordance wi th Dutroulu,
that tenesmus occurs chiefly in gra,ve cases in which
there is extensive sloughing, burning sensation in the
rectum and anus during and after pa.ssage is very generally complained of.
Nausea and vomi ting occur especia,lly at the onset,
but occurs in many instances at irregular intervals during the course of the illness.
The ingestion of food
and in the case complicated with liver abscess and lung
abscess, paraxysmal coughing may occur.
Elevation of the body temperature is not a prominent feature in this form of dysentery, which in this
respect is similar to other forms.
It is,never the less, true that if careful observB.tions are ma,de, an elevE tion of temperature above the
-
normal point will be found at some period of the twentyfour hours daily throughout the period of the illness.
-25-
Exceptions to this must be made in severe gangrenous
dysen tery, in which the temperature is sometimes norma.l
or subnormal for twenty-four hours or more, and in chronic dysentery, which may be absolutely afebrile for days
or weeks.
An exacerbation of dia.rrhea. may be accompanied by
slight increase in fever, but is not at all constant.
The accompanyment of Ii vera./'Ir/ lung abscesses produce
an elevation of tempers.ture.
irregular.
The temperature curve is,
There may be alterations of continuB,tions,
remi ttent pyrexia. throughout the illness and this occurs independently of any complications.
As convalescence is established, the fever declines
through slight irreguls.r elevations of temperature have
been seen even when die.rrhea, is absent.
The Beverage
range of temperature in uncomplicated cases is from
99°-101° or 102 0 F., ~md evening temperature is usually
higher than morning temperature.
Rigors do not occur in cases which are uncomplicated, such as cases of liver abscess.
Sweating is observed in all abscess Cases and in
ga,ngrenous dysentery is often associated wi th a subnormal tempera.ture and feeble circulation.
cases of dysentery it is seldom seen.
In moderate
In chronic cases
the skin is persistantly dry.
Circulation and respirations are affected in the
-26-
same degree that they are·in other diseases attended
by modera.te pyrexi a.
Wi th the abrupt ons et there is
accentuation of the pulse which ranges from 80 to 100
and is full and regular.
out the disease in
90.
The
most common rs"nge through-
uncomplicated cases is from 80 to
In gra,ve cases, 100 to 110, whi Ie in chronic oases
the pulse rate only ocoasionally exceeds the norma,l.
With progressive exaustion in the fatal cases, the pulse
becomes feeble, compressible and more rapid, ranging
from 120 to 140.·
The respirations are increased in ratio with the
pulse.
The condition of the circulation a.nd respira-
tion in cases complicated by hepatic and pulmonary abscess is considerably more rapid.
The urine is usually slightly a.ffected in all
cases, having some albuminuria,.
There is usu8"11y no
disturbance in kidney function in cases of chronic
dysentery.
In ga,ngrenou6 cases, there may be reten-
tion, quantity very slight, and urine highly concentrated.
-27-
Complications
Abscess of the liver is one of the most common
and serious complications of amoebic dysentery.
It
developes in about twenty-two per cent of the cases
of amoebic dysentery.
male~more
It is much more frequent in
common in foreigners ~O the tropics than
in the natives, and rare in children under ten years
of age.
It mas develope at any time during the course
of the intestinal infection.
Not uncommonly it occurs
after 8,,11 symptoms of dysent ery have ceased for a. long
period of time, or sometimes before s"ny noticeable intestinal symptoms have developed.
,-
In some fS.tel cases
of liver abscess there have been no evidences of intestinal lesions at autopsy and no history of dysentery
during life.
A history of dysentery may, however, be
obtained in about sixty to ninty per cent of the oa.ses
according to some statistics.
In the majority, the
abscess becomes evident in the first month after the
onset of the dysentery (14).
The use of alcohol in
cases having amoebic dysentery, seems to be a predisposing factor in liver abscess as well as other dieteticiexcesses and exposure.
The most common seat of the abscess is the upper
and posterior portion of the right lobe of the liver.
In the greatest me.jori ty of cases, only one abscess
is found, but multiple abscesses are seen in some cases.
-28-
Rarely, as many as two or three hundred small abscesses
ma.y be found.
The amoebae usually invade the liver by
way of the portell vein and these parasites are frequently found lying in the veins of the submucosa and in the
portal capillaries and veins.
In about half of the ab-
scesses bacteria may be obtained by culture.
The re-
mainder are sterile in regard to microorganisms. The
small amoebic abscesses consist of thick glairy, yellowish masses of mucus which are not fluid.
In the large
abscesses the contents are more liquid and of a creamy,
gelatinous, purulent consistency.
In color they are
yellowish, grayish red, brownish red or greenish from
the adjacent mixture of bile.
Shreds of necrotic liver
tissue B,re mixed wi th the fluid portions.
Microscopi-
cally, one is struck usually with the absence or presence
in ae small number only, of polymorphonuclear leucoeytes.
The contents consist of granular material, consisting
of fragments of cells, SWollen degenerated liver cells,
red blood corpuscles, fat globules, cholesterin crystals a.nd amoeba,e.
The amoebae are sometimes difficult
to find in the pus, but can almost always be found in
scrapings from the wall of the abscess.
In abscesses where no bacteria are found, you
find that the amoebae have c!tusea necrosis and liquifa,etion of the tissues wi thout
matory reaction.
-29-
any
pronounced inflam-
In the very early abscesses you may find liver
cells still present.
There is edema of the surround-
ing tissue a.nd there are
a~
few m(monuclear phagocytic
cells in the neighborhood.
Symptoms and Diagnosis of Liver Abscess. (15)
The condi tion ma.y develope very s lowly and for
this reason is frequently overlooked, and perforation
may be the first indic8ction.
Inli ver abscess there
is no single symptom that is constsont proof that the
liver is involved.
The general condition and appear-
ance of the case may lead to the diagnosis, which sometimes is confirmed by aspiration.
A history of previous
diarrhea may suggest the condition, but an absence of
such history can not exclude such a diagnosis of liver
abscess.
If the onset is accute the diagnosis is made much
more readily.
Rogers recognizes a stage which he terms
pre-suppurative stage of amoebic hepatitis in Which
amoeba.e from dysenteric lesions have lodged in the porta.l capi llaries of the li ver, but Rctu.l abscess has
not taken place.
There may be a low remittent fever
anct a leucocytosis in Which the polymorphonuclear leucocytes are increased very little in per centage.
He
thinks at this time the administration of emetine may
prevent liver abscess formation.
-30-
In differentiating
between the pre-suppurative end suppurative is often
very difficult without puncture and this sometimes is
very unsatisfa,ctory.
If chi lIs and swee.ting a.re pres-
ent and the condition does not improve by emetine,
suppuration may be expected.
Fever, pain, enlargement and functional disturbances are the more frequent indications of liver abscess.
Fever is usuB,lly present at some time, but is
often insufficient to attract the attention of the
physician.
Sometimes it is irregular, from 9.9.0 to
102 0 F., and it may be of a septic type rising in the
evening to 103 0 to 104°.
Chills and fever may occur
and the symptoms resemble,more or less, maleria. Sometimes the conjunctiva Shows a slight amount of jaundice,
and persistent vomiting ma,y occur (16).
In certain cases the facies may suggest the diagnosis; emaciation occurs in some cases, and the appetite is poor and the tongue becomes coated and fuzzy.
Pain is a variable..
It ma,y occur in the right
shoulder when due to irritation of branches of the
phrenic nerve, or over the hypochondrium. or epiga,strlum.
When not present spontaneously, it may be elicited
on pressure over the liver.
Enlargement may be detected
by physical examination or by x-ray.
is usually upward
8.Tld
The enlargement
may reach as high as the angle
of the scapula, or it ma,y progress so as to cause a
-31-
bulging on the right side, a, swelling may also be seen
over the sixth and seventh rib in some extensive cases.
The movement of the right side of the chest during
respiratian may be linli ted and the right rectus may
show some rigidi ty.
Percussion a.nd auscultation fre-
quently give no information of the condition.
You may
get an increase in hepatic dullness.
Functional disturbances may also be associated in
making a diagnosis of liver abscess.
When considerable
destruction of the hepatic substance has taken place,
the area of excretion may be diminished.
Stitt believes
that the most specific test for liver function is to be
that of urobilin.
The per centage of ni trogen elimina.-
ted as ammonia may also be increased in diminished liver
function.
An absolute diagnosis can often only be made
by aspiration and finding the Entamoeba histolytict=t in
the pus.
Lung abscess is next in frequency to liver abscess.
I t may be secondary to a Ii vel' a.bscess developing from
direct extension, or it may occur primary.
The amoebae
entering the lung through the hepa.tic veins.
The abscess
is very similar in character to that of the liver.
The
formation of a.bscess ms_y be preceded by a"n irregular
fever and an irri ta.ting cough.
Respirati ons are fre-
quently increased in number and shallow.
-32-
Pleursy usu-
ally precedes perforation.
toration appears.
Cough appears and expec-
When the abscess ruptures into a
bronchus, the respirations become less frequent
a definite sputum is found.
sa.uce-li·ke sputum.
a~nd
It is called ancnovy-
The abscess may continue to dis-
charge for years or death may occur in short time. In
favorable cases, it may cles,r up in a few months, but
the prognosis in these cases is very much guarded.
Peritonitis.
Peritonitis is a quite common com-
plication in amoebic dysentery_
Local peritonitis may
result from extension of inflammation from the ulcerations in the intestinal wall until the peritoneal coat
is inva,ded with deposition of lymph, fibrin, a.nd other
inflammatory products on the surfa,ce.
Ps,tches of fi-
brous adhesions are frequent in chronic cases.
These
ma.y cause abdominal soreness and pSoin.
Peritonitis which generally proves fatal may follow perforation of a. liver abscess or of an intestinal
ulcer.
Perforation of an ulcer usually results from
a deep sloughing ulcer.
It has occurred in the cecum
and has been mistaken for appendicitis.
.
Perforation
occurs in only about three to four per cent of the
cases which are hospitalized.
fatal when it occurs.
It is almost always
Perfo:r:ation may also occur retro-
peri toneal and a,ffect the psoa,s muse Ie a,nd abscess wi 11
point in the inguinarregion as s, psoas a.bscess.
-33-
Amoebic appendicitis has been identified, but is
very difficult to make a definite diagnosis in the
living.
It is usually an extension from the cecum (17).
Brain abscess is a very serious complication and is
always fata,!.
li terature.
There are many cases reported in the
Kartulis reported severa"l cases found in
the literature.
In reviewing case reports, all the cases but one
had occurred in the cerebrum either in one hemisphere
or the other.
The abscess are usually Single, but may
be multiple.
The fluid in the a,bscess appears similar
to that of the liver.
It is usually reddish brown and
contains necrotic brain tissue Bond thrombosed blood
vessels attached to the walls.
The meninges are seldom
affected, therefore, a lumbar puncture will yield a
clear :fluid.
The toxic evidence of suppuration are
not prominent and there is usually little or no evidence of intracranial pressure.
The disease proceeds
rapidly and death occurs usually within six to ten days
after onset.
P!:ttient loses consciousness and coma
pidly develops.
1'8,-
If the abscess ruptures into the ven-
tricle the course is very acute.
Oonvulsions may occur and the temperature may rise.,
Some Cases go into a sudden mania, others develop coma
wi thout any previous symptoms.
-34-
Os_ses have been reported
where Jacksonian epilepsy was the first symptom.
rne
usual methods used in diagnosing brain abscess or tumor
is much help in some cases.
Arthritis deformans has been recently worked out
and reported by Eby, Reed, Wycoff and Kofoia (18) as
a complication of amoebic dysentery.
They have re-
ported the finding of amoebae in the joints of CB.ses
with arthritis deformans during amoebiasis.
This has
not been generally accepted by the medical profession
as yet, but is a subject which is well worth considering.
-35-
Etiology and Diagnosis
The diagnosis of amoebic dysentery is very difficult in some cases, E'Jld many times it is only made in
the laboratory.
There are many other forms of dysentery
which resemble the clinical picture of amoebic dysentery
very much.
It is possible to differentiate bacillary
from amoebic by the more sudden and acute onset of the
bacillary type together with fever and other signs of
toxemia.
The pulse rate is definitely more rapid in
the baci 118ry type tha.n in the amoebic tyJ.:e.
The number
of stools being more frequent and less in amount. (19).
The diagnosis (20) in any case of amoebic dysentery
should be confirmed by the finding of the amoebae in
the stools, or the typical four nucleated cysts which
are characteristic of the Entameba histolytica.
The
examination of the s tool should be made a,s soon as possible after the s tool has been passed.
I f the s tool is
allowed to stand the amoebae soon die or cUsentegrs.te
and are not found on examination.
If you want to keep
the BJlloebae li ving you should have a heated substage
Which keeps the amoebae 8.11 va and aui te actively motile.
In studying the living amoebae you must have them alive
and motile, then they will not be mista,ken for a pha,gocytic cell.
.-
After the amoebae h8.ve been demonstrated
to be alive and B,cti ve, the clinicit:tn should be a.ble
to differentiate the three most common amoebae found
-36-
in man.
The distinction between these amoebae is very
difficult in many ca,ses lind the experience of the clinician is very necessary_
The most popular
be~ief
of
the men having a great deal of experience in the observation of amoebic dysentery say that, Entamoeba
histolytica is the only one which ingests red blood
cells, and when a,n amoeba is found to have ingested red
blood cells it is quite'conclusive that it is Entameba
histolytica.
Many men debate this previous statement
and say that L4max a,nd Enta,moebe, Coli will 8.,lso ingest
red blood cells.
The distribution of the chroma,tin in the nucleus
is frequently 'of aid in a1 fferentiation.
The examine,-
tion of cysts in stained preparations gives more accurate results in the determination of species.
In staining the cysts, there are many methods.
Scha,udinn's method which is an alcoholic sublimate
'iron hematoxylon.
Donaldson's method is mOl't success-
ful; he used iodin eosin solution..
freshly prepared.
This should be
I t is made up of a sa,turated solu-
tion of eosin in normal salt, two parts; five per cent
potaSsium iodid,e in normal sa,lt solution, two parts.
The smear is prepared, by rubbing out a minute portion
of the feces by rolling it around an applicator stick
in a small drop of normal saline soluti on, then a,dd a
drop of the iodin eosin stain.
-37-
The cysts stand out
clearly a,s bright spherules which soon become tinged
with the iodin to varying tones of yellow, while their
glycogen filled vacuoles, when present, turn light or
dEtrk, brown a,ccording to their mass.
The nuclei become
more clearly defined Bsthe iodine penetrates, especia,lly in Entamoeba histolytica and Entamoeba coli.
In the Endalimax
/
'-1'~
na~'3"
they are detected with difficulty.
cysts o'f Entamoeba histolytica measure from 5 to
''-''';
20 /~~\\ on the average.
\
They are spheri calor ovoid,
·,\">....~~I
and the cyst wall is clear Etnd perfectly smooth a.nd is
formed of a, single layer.
When the cyst is first formed it has only one nucleus and it measures about
on~-third
the size of the
whole cyst.
The cysts are passed in the feces in the uninucleated, binucleate and quadranucleate stages.
~-"",The
r
cysts of EnteJnoeba coli measure from 10 to
\
3d. cc.) or more.
\ .."
The cysts containing one, two, four
/'
or eight nuclei may occur in the stool, the cysts cont cdnlng eight nuclei when mature.
It is conSidered
that 80 per cent of the cysts found in the stool ha,ve
eight nuclei.
The mature cysts of Dndalima"x nana are typically
oval and measure usually from eight to ten microns in
length and seven to eight in width.
Kofoid and Wenyon
believe that the structure of the nucleus of Endalimax
-38-
nana when stained is an absolute diagnostic criterion
of this species.
In Entamoeba histolytlca there is a centra,l karyosome and the peripheral chromatin is scattered over
the nuclear membrane in gra.nu1es of a small size, whereas, in Endalimax nana there is no centra,l karyosome and
the peripheral chromatin is massed in a single large
clump at one point on the nuclear membrane.
Hegner and Cart (21) made out the following tr:tble
in 1921 which differentiated the three main types of
amoeba in man:
Chara.cteristics Enta.moebe" Hist .Enta.moeba Coli. Endalimax nane
Uns tained B.li ve
Size
Small 5-30u
Ingestion of
corpuscles
common
Shape in motion One pseudopodium protruded
in direction
of movement.
Locomotion
Active ,pseudopdis protruded
explosively.
Large lO-30u
ra.re
One pseudopodium protruded
in direction
of movement.
Sluggish,pseudopodia. formed
by/flowing out
slowly.
Endopl!'tsm small
Ectoplasm is
strongly rein amount;less
fractile, end- refractile;enoplasm finely do plasm vacuogranular.
lated.
Stained in iron Ohroma,tin: a
ChroIDl:ttin: a
hematoxylin
small central larger central
granule and
granule often
many small
eccentric, B.nd
gre.llules on
many large
nuclear memgranules on
br~me .
nuclear membrane.
-39-
Very small 5-15u
rare
One or more small
pseudopodia at
one time.
Sluggish in formed stool, active
in liquid stool.
Endoplasm very
clear and refractile.
Chromatin: no
central gr~mule,
large mass and
one or more
smaller masses.
In many cases of amoebic dysentery it is very
difficult to demonstrate the protozoan as being present in the stool a,nd the cysts are also very difficult to find in many cases.
~lhere
the most difficulty
is found is in the chronic cases and during the remissions,and also in cases of suspected carriers.
There-
fore, I think that John Gordon Thomas has outlined a
method of which should be observed in sending stools
for examination.
The first point he brings out is that
the whole stool should be sent when possible.
This is
of aid, since the general appea,rance of the stool is
frequently characteristic.
Thus the parasitologist
can see at a glance whether the stool is diarrheic,
semi-solid, normally formed, or constipa,ted, and whether mucus or blood are present, and is so in what
quanti ty.
Next, the s tool should reach the labore,tory
as soon
possible.
B.S
The vegati ve stage of amoe-bEte
is greatly affected by adverse circumstances.
The ac-
ti vi ty wi 11 be present only at a tempera,ture of a"bout
37 0 C.
T'ne amoebae become rounded up and immobile,
but become active somettmes when a Warm stage microscope is used.
Cysts withstand external conditions
much better, but often a short period will cause them
to become degenerate a,nd more difficult to diagnose.
When the entire stool cannot be sent the clinician
-40-
should carefully select the portion from the stool
which is called Sago-grains or nodules of mucus.
A
platinum loop full may contain hundreds of amoebae,
where the remainder of the stool may contain only a
few.
The macroscopic appearance of an amoebic dysentery stool is quite characteristic.
In the exacerba-
tion period, it may contain only blood a.nd mucus.
It
should be noted that the general color of the stool is
a reddie.h brown, or, as it has sometimes been described,
chocolate shade, and not bright as ordinary blood.
The stool may be a fluid in which the mucus is
so intimately mixed with the fecal material as to be
almost imperceptible to the naked eye.
commonly present.
This, is not
The stool may consist of mucus in-
timately mixed with the fecal material in which the
mucus is seen a,s small masses or blabS so a,ptly described as "Sago grains" appearance.
In the more latent
cases the stool if formed of normal consistency and to
the naked eye presents only one fea,ture, unfortunately
not alwe.ys present, which e,re small glistening pin-points
of thick tenacious mucus on the surfa.ce.
In ma,ny of such
cases the stool appea,rs to be perfectly norma,l, but mrmy
variations may occur, such as the sudden passage of pure
blood from an eroded artery.
-41-
In many
incid~nces
it is necessa,ry to use a saline
cathartic the night before and produce a liquid stool
before the amoeba.e or cysts may be found in the stools.
In questionable cases where the diagnosis is difficuI t to make and the amoebae a,re not found or may be
present and not distinguishable from the Entamoeba coli,
i ~ becomes necessa,ry to use a proctoscope or
a~
sigmoid-
oscope and frequently the ulcerations will be seen in
the sigmoid or descending colon.
By the use of a long
applicator swab, wipe out one of the ulcers thoroughly
and, in many insta,nces, you wi 11 find the acti va amoebae
if examined immediately.
I think this proc.edure is of
great importance in many auestions. ble cases where the
amoebae are not found in the stools.
A complement fixation test has been worked out by
Dr. Cha.rles F. Craig (22).
This is a method very simi-
lar to that of the complement fixation test of syphilis
used in the army.
He uses an alcoholic extract of the
cultures of Entamoeba histolytica grown on a. modified
Boeck-Dibohlav medium and develops until there are availEtble at least one hundred twenty culture of organisms
/
for eBtraction wi th a,bsolute alcohol.
It is necessary
to use great care in titrating this antigenic extract
from hemolytic qualities, anticomplementary qualities
and antigenic strength.
The technic of the test is
important and should be attempted only by a trained
-42-
serologist.
The practical value of the test, there-
fore, is limi ted Pflrticu1arly by difficulty of PI' epa~r­
ing and titrating the antigenic extract.
Craig des-
cribed this technique in September 1929.
He reports
it is of value in diagnosing cases of amoebic abscesses
of the liver which has no intestinal symptoms and in
diagnosing hea.lthy carriers wi thout symptoms.
The test
is the strongest in cases of carriers and mild infections.
In some acute cases it is negative or doubtful. The test
is not positive with other species of amoebae of flagellates.
Normal persons or those ill with other dis-
eases do not give positive reactions.
The complement
fixation bodies disappear from patients' blood serum
after antiamoebic treatment and the disappearance of
Entamoeba histolytica frcm the feces.
It is positive
during relapses, unless repeatedly negative for severa,1 weeks.
Therefore, a negati ve rea.ction does not
prove the absence of amoebic infection or the.t antiamoebic treatment has resulted in a cure.
It is thought by many clinicIans that this test
is of little value due to the fact that the Entamoebae
lue so difficult to culture and the antigen and com-
plement is so difficult to titrate.
Also the test does
not give a positive reaction in a great enough per centa,ge of Cases to make ita test of any great diagnostiC
vEllue.
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Treatment of Amoebic Dysentery
In the treEttment of amoebic dysentery the patient
should be put to bed and kept in bed all the time during treatment.
In the past century there has been
many methods of treatment introduced which indicates
tha.t there is no one treatment which wi 11 give a positive cure.
Emetine (23) has become the most efficient trea.tment in late years.
Ipecac was formerly advocated for
treatment regardless of the
c~mse.
The Brazilian root
waS first taken to Europe by Fias in 1658, where it
was successfully used by Helvetius in the treatment of
Louis the XIV and was sold a.S a secret remedy to the
French government.
Two centuries later, Docker intro-
duced the use of lctrge doses, 60 gr. two or three times
a day, of powdered ipecacuahae in the
vere dysentery in Mauritius.
trea~tment
of se-
His excellent results
were confirmed by others.
In 1886 Msoclean s.nd Chevers (24) a,dvocated the use
of ipecac in acute hepatitis.
Later the drug fell in-
to more or less disrepute, but its use has been reserved
as a result of Mansonts advocacy of its employment in
dysentery and Rogers in hepatitis.
Meanwhile, many
other drugs have been used in dysentery, such as quinine, bismuth, tannin, salines, opium, salvarsan which
-44-
-.
have been given in all methods.
The chief interest in the treatment of amoebic
dysentery is centered around ipeCEtC and its deri vati ves,
emetine being the most efficient.
The drawback in its
use is first the reaction received and by the fact that
some cases do not respond.
Epecac contains ii ve
~dka­
loias of which emetine and cephaelin are the chief ones.
In 1912 Vedder (25) reported the effect of ipecac on
amoebae and this showed that emetine killed amoebae in
a dilution of 1-100,000.
From this work he concluded
that it waS a very good amoebacide.
Following this
Sir Lenard Rogers, in India, tried hypodermic administration of emetine and reported strikingly good results
espeCially in early acute cases.
Charles F. CrEtig (26) recommend.s particularly the
use of emetine hydrochloride or emetine bismuth iodide.
Emetine is speci fic for the relief of
s~Tlnptoms.
The
symptoms are reb.eved in the first few days a,fter beginning administration.
It is doubtful if it actua.lly
cures over one-third of the cases.
They are always
subject to recurrences and the word cured should be
guarded against very carefully.
The drug may be given orally, subcutaneously or
even intramuscularly.
The patient gets cui te a rea,ction
out of oral S,dministration s,nd nausea and vomiting is
qui te common.
When given intramuscularly or subcuta,ne-
-45-
oU81y, the patient gets considera.ble pain and soreness
at the area of injection.
When given orally, it must be given in a leratincoated pill or capsule so that the drug is not
a~bsorbed
in the stomach, but passes into the small intestine before the keratin coat is dissolved.
siderable gastric distress.
This prevents con-
The dose for ora.l adminis-
tration should not be more than a grain and a half at
morning and night in equally divided doses.
It is seldom
used by mouth a.lone, but with subcutaneous or intra.museular injections, one-half gratn given by mouth and one
gratn by intrainusculS$r injection every morning for ten
to twelve days, repeating this treatment if relapses
occur.
Emetine is a toxic drug and when given in too la.rge
doses, Causes severe diarrhea, myocs.rdi tiS, neuri tis,
nervous prostration and great musculs.r wee,kness.
may occur suddenly from cardiac failure.
Death
These symptoms
should be consta,nt ly watched for when the drug is being
given.
If such symptoms develop the drug should be
stopped at once.
Peripheral neur! tis (27) after trea.tment wi th emetine is quite common.
The trouble USUE:tlly manifests
itself in general muscular pa,tn and weakness, especially
in the legs and sometimes going on to paresis.
and toe drop is quite common.
-46-
Wrist
These symptoms gra.duB,lly
disappear after stopping the emetine.
There has been
many cases of death from emetine poisoning.
In many
of the cases reported a,s small a dose as four gra,ins
sprea,d out in equal doses for four days.
The toxic
symptoms a,.re first manifested by dia,rrhea and muscular
weakness, and the heaxt becomes very weak with the usual cause of death being cardiac fei lure.
In ca,ses in which a, course of emetine treatment
has been given a.nd the patient received no relei f, emetine has been stopped a.nd chapparo amorgosa used.
drug was introduced by Wenyon and OIConnor.
is administered
Q6
Thi s
The drug
a glass of fresh infusion fo llr times
a day, a.nd a, quart of the Same infusion by rectum aiter
a preliminary injection of sodium bicarbonate solution,
one ounce to a Quart of water.
Sellards and McIver have
reported successf'ul treatment of four cases with this
drug, but this treatment has been nearly forgotten in
recent years.
Sodium iodoxyquinoline (28) sulfonate (Chinioform)
may be given orally or as enema in treatment of acute
amoebic dysentery.
In the adult the drug is given one
gram three times a day for eight to ten days,
If this
causes diarrhea, reduce the dose to one half.
The enema
given is made up of about 200 co. of warm 2 per cent
-
solution of chinioform which should be reta.ined for several hours.
This is given a,long wi th oral adminlstra,-
-47-
tioD of seven and one-he,lf grains three times a
da~y.
Chinioform is less toxic and is apparently just as
effectige as emetine hydrochloride or emetine bismuth
iodide.
Oil of Chenopodium (30) has been used in treating
many cases of dysentery.
It waS first found to be of
value when Mendelson used it for the treatment of hook
worm) and he noticed that the patients with dysentery
were much relieved in many cases.
From his investiga-
tion he found that oil of Chenopodium was
8.
very good
amoebacide.
Drs. Walker and Emrick also did considerable work
on
a~oebic
dysentery carriers in 1918.
It is very im-
porta,nt to treat cacrriers due to the fact that the carrier is the most important factor in the control of the
disease.
carriers.
Emetine is not satisfactory in many cS,ses of
A satisfactory treatment of carriers of Enta-
moeba histolytica, not only must be capable of destroying
the intestinal parasites, but also it should not occupy
too much of the patients' time.
The method of treatment outlined by Walker and
Emrick was to give the patient first, magnesium sulphate-,
from one-half to one ounce B.t 6: 00 8.m.; second, 01 I of
Chenopodium, 16 minims in a keratin caps.ule or gela,tin
capsule at 8:00 a.m., 10:00 a.m. and 12:00 m.; third,
castor Oil, one ounce.
This dose is for adults. Children
-48-
should have the dose regulated according to the age.
The oil of chenopodium is given shortly after the purge,
so ths.t it will reach the intestine before the amoebae
become encysted.
If a single course doesn't result in
a cure, then repeat again after a one-day interval.
The most importa.nt thing in this treatment is to
be sure the purge is of sufficient quantity to produce
a liquid stool.
This also cleans out the bowel a.nd
gives the drug a better chance to attack the paraSites
and also there is less dilution.
Drs. M. E. Baines and E. C. Cart (31) introduced
the use of oil of chenopodium in an em,ulsion of gum
acacia by rectum.
In the use of the enema, the rectal
mucosa should be protected with petrolatum.
The dose
of the inert oil should be limited to two ounces. The
buttock should be eleva,ted and the enema gi ven slowly
and with great care.
The first dose should not exceed
eight ounces in the adult.
The enema should be retained
for an hour or two if possible.
Dr. Mason recommends giving the oil of chenopodium
in two ounce doses of inert oil in six to eight ounces
of olive oil.
This drug is toxic in over-doses and should not
exceed the normal dose.
th~ln
It should not be given in less
ten days to two weeks a,fter a. full dose is gi ven.
An over dose is toxic end causes kidney damftge and should
be watched very closely.
-49-
Oil of Chenopodium relieves promptly the clinical
symptoms in many patients with chronic and subacute
dysentery.
It is safely B.dministered with castor oil
when given orally.
You may give the drug to the patient
and let him take it by himself.
-50-
Summa,ry
In slllllmarizing amoebic dysentery, I find that
the history of dysentery goes back ma,ny centuries, but
its etiologics.l pa,rasi te was not discovered unti 1 1859.
and not recog'nized or connected wi th the ca.use of dysentery until 1875.
The definite pathology was first writ-
ten by Councilman and La,fleur in 1891, and it wa.s not
until 1903 when Schaudinn gave the orgenism the name
Entamoeba. histolytica and proved it to be the etiological factor in producing one type of dysentery commonly seen in the tnopics.
The symptoms of the disease may be sudden in onset
or very insidious, or may never show any definite symptoms.
In acute attacks the dysentery is one of the
outstanding features and the appearance of the stool
is of much significa.nce.
Tl1e patient also has a,bdom-
inal discomfort and tenderness over the colon.
In in-
sidious cases you may have no symptoms that are definite.
The dia,gnosis is made upon finding the amoebae or cysts
in the stools and upon observation of lesions in the
colon by proctoscopic examination.
In some cases the
clinical history is sufficient to ma,ke a diagnosis, but
it should be confirmed by finding the trophozoites or
cyst forms.
The complement fixation method is not
definite enough to depend upon, and culture methods
-51-
are very unsatisfactory and difficult to handle.
The treatment of this disease has been very vEl,riable.
Many drugs have been used in treatment of amoebic
dysentery, but at present there are only two drugs commonly used.
One is emetine, which is given intramuscu-
larly in the form of emetine hydrochloride, and orally
in the form of emetine bismuth iodide.
The other drug
is Oil of Chenopodiu.'U which may be given in gela.tin
capsules or in solution of oil as an enema.
Both drugs have given very striking results, but
the patient is still subject to remissions, and a cure
should never be promised when starting to treat a patient with amoebic dysentery.
-52-
Bibliography
1. Garrison, History of Medicine, 1924.
2. Review of the Recent Work on }~oebic Dysentery,
Boston Medical end Surgical Journal 183: '20.
3. Councilman, W. T. and La.fleur, H. A.,
Johns Hopkins Report, 1891.
4. Sajoresi;s Analysis Encyclopedia of Practical Medicine
Vo 1. I I: 370, 1919. .
5. Journal American Medical Association, 101. Pt.2:2068.
6. Kofoid and Swezy, Journal American Medical Association
78: 1925.
7. Boetjer, W. A. and Sella,rds, A. Wq
Bulletin Johns
Hopkins Hospital, 25:165, 1914.
8. IdentificEttion of Entamoeba Histolytica, Journal
American Medical Association, May 3, 1913.
9. Hegner, Robert, Study of Amoebiosis in Panama,
Journal Pe,rasi tology, M~!'rch 1932.
10. Antigenic Properties of Free-living and Pathogenic
p.moebae, American Jour. Hygiene 16:97-123 July '32
11. Amoebic L'Ysentery, c.Tournal Amerlc8<n Medical Association, Oct. 19, 1933.
3. Councilman, W.T. and Lafleur, H.A.,
Report,
2:395, 1891.
Johns Hopkins
12 .. Boeck, W.C. and Drbohlor, J., America.n Journal
Hygiene 5:371, 1925.
3 .. Councilman, W.T. and Lafleur, H.A.,
Report.
Johns Hopkins
14. Nelson Loose-leaf MediCine, II p. 331.
15. Diagnosis and Treatment of Amoebic Dysentery, Journal
P.merican Medical AEsociation, May 3, 1913.
16. Sellards, 'I.W. and Theiler, M., American Journa.l
Tropical Medicine, 1924.
17. Symptoms, Diagnosts and Prognosts of Uncomplioated
Amoebiosis in TropiCS, Journal American
Medical Association, 45:830, Sept. 6, 1905.
-53-
18. Key, Reed, Wycoff' and Kofoia, AmoebiaSis in Relation to Arthritis Deformans, California
Medical Journal, 1925.
19. Proc. Roy. Soc. Meo. (Tropical Medical Section),
24:46-56, Sept. 1931.
20. Proceedings of Royal Society of Medicine l4:pa.rt 3,
1920-21.
21. Hegner, R.'1f. and Cart W. W., Die.gnosis of Protozoa
and Warm Parasites in Man. Baltimore 1921.
22. Craig, C. F.,
Journal American Medical Associ a.tion
January, 1931.
23. Dale, H.E. and Dabell, C., Journa,l Pharm. 8"nd Exp.
10:399, ,Dec. '17.
24. Ibid.
25. Vedder, E.B., Far Eastern Association Tropical Medicine trans Congo p.S7.
26. Craig, C.P'., Diagnosis and Trea.tment of Amoebic
Dysentery, American Jour.
January 1913.
Medica~_$cience
27. Emetine Due to Peripheral Neuritis Following Amoebic
Dysentery, Kilgore, Boston Medical and
Surgery Journal, 175:380.
28. Ibid.
29. Wenyon, C.M. and O'Connor, F.W., Human Intestinal
Protozoa in Near' East, Bureau Scientific
Research, 1917.
30. Walker and Emrick, Treatment of Carriers of Entamoeba histolytlca with Oil of Chenopodium.
Journal American Medic~ll Association,
68:1456,
1917.
31. Ba,rnes, M.E. and Cart, E.C .. , Oil Of Chenopodium in
Treatment of Amoebic Dysentery.
,-54-